I like to start as promised this thread to discuss or debate somewhat deeper than just to show how we can collect MOXY/NIRS data's and what we can read out or may be able to read out.

There are some very specific point who motivate me to take this intriguing topic on here. As most regular readers know by now, that I am not able to make cook book or recommendation as a general recommendation, as I do not believe we are abele to get this right. The problem we create is, that many out there see, that NIRS could be a great additional tool to make some differences form what we do , taking % of something ) and replace it with some more individual feedbacks. What they all ask us in many discussions and e mails is a very simple to understand concept. We than try to deliver that and show a " zoning " idea including where we see the potential current assessed limiter and or compensator. Now the problems start on two fronts. a) the coaches are than not happy as they like to k now more into details where and how we find this limiters and compensators. So they do not like the approach we all accept with an y critic the % cookbook we all sue whether we believe in VO2 max LT or FTP or what ever. We get the result than we take a calculator and get the zoning without any critical discussion or questions. Now when we offer the same approach we immediatly get the accepted and well taken critical question, that they like to know how we made this conclusion. ??? double standard ?>??? Than as soon we offer or try to show how the different physiological system may interact we have the problem , that many of the current believes are getting a critical review and that's where we often than get stuck.

So I hope on here to get people interested in some intriguing ideas and we try to back them up as good as we can to engage in a debate here and come back with questions but we may not always have the answers. So here 3 motivator to start this thread. 1. Sandy and Rachel foremost as they give me the chance to use outside information to show weakness and strength of NIRS assessment combine d with as much other ideas we can get and or afford.

2. Ruud. with this section here.

Ruud

I know that these things are scattered around the forum and if you look closely you will see there often is this kind of structure. But given my own experience (almost a year now) it is sometimes hard to find that structure. Not a critic, but just to help.

and by

Ryinc

Based on the information, you posted, thinking out loud I think the answers are:

If you wanted to get more O2 from the lungs to blood, in effect you want the disscurve to shift left, which increases O2 affinity/stickiness. One way to do this would be to reduce C02 which (in theory) can be achieved by breathing intensely (i.e. opposite of holding your breath)

If you wanted to get more O2 from the blood to the cell, in effect you want the disscurve to shift right, which reduces O2 affinity/stickiness. One way to this would be to increase CO2 which (in theory) can be achieved by holding breath for longer

Unfortunately don’t have Moxy yet, to try the experiments above. Again, if the answers above are correct, then I am confused about the case of top endurance athlete (and for which Rachel's picture is similar according to her) where SmO2 values are persistently high implying that transfer of O2 from lungs to blood is good, but transfer from blood to muscle cells not as good (as this would imply CO2 too low, not CO2 too high).

and this section here

Can you or Jeurg ( or anybody else) elaborate on some further ideas on the types of training and tools that you would use in instances of other limiters. The intention is not to create a "cook book" as Jeurg would state it but i am trying to understand some practical examples of how one might say train cardiac system without stressing respiratory or muscles. Or train, muscle strength without stressing other systems. Or more generally train utilisation without stressing delivery, or train delivery without stressing utilisation?

So the next thread I try to start to get directly into this point using Rachel's assessment information.

In the first overview or first glance when looking at this data.- 50 +- % resting SmO 2 with an incredible fast increase to a very high level and than minimal change even at the end where Rachel for sure worked hard perhaps even very hard. and we have some confirmation based on her HR at the last stages.Just or fun short feedback on HR at 480 time marker we have an interesting step and perhaps starts where Sandy decided to make a different step as it may otherwise go far to long to get her to the end of the assessment. ?- SmO2 trend in a first spontaneous thought.

a) This looks like we often see, when we have a non or minimal involved muscle included in the assessment. So great delivery and no real demand of O2 and only depending on systemic limitation we will see a change towards the end with a drop in tHb and SmO2. This we still have to look at. Now vastus lateralis in ultra long distance runners are very efficient in striding and have a very small activation on vastus lateralis and even less, if they are heel striker.Mount a MOXY at gluteaus maximus and see whether this is a runner with more work from hip rather than from a load in knee extension and very minimal eccentric quadriceps activity. b) incredible good delivery so great cardiac out put and good respirationc) not great feedback due to positioning and so on. But for this we simply add the needed thB anyway. So below a closer look at SmO2 and tHb of the full assessment length

The thB shows a very nice great trend where we see 1 min stops and new starts to the loads. So good data collection and what we see is real Now here the first feedback needed to see how we look at this info.

tHb trend. ( not absolute numbers or not a specify value just trend. Question : What reactions or activities s will influence tHb. I try her to start with the first few basic reactions we may see to keep it on a level we all can use as coaches and athletes. I may miss some but that is okay and question will come up.

1. Start or resting tHb in the one minute calibration time is an indication of the current blood flow or blood volume in the area where we fixed a MOXYMain reason why tHb increases in a start phase is : vasodilatation effect due to alarm phase.- Increased blood flow due to increase in cardiac output. So both will indicate an increase in blood flow. and a third one is an increase in capillary blood flow ( will be a hard discussion later ) Against an increase in tHB or blood flow is the mechanical compression due to a muscle contraction.Now mechanical reactions are now . systemic reactions often have lag time. So look at the start ' tHb drop due to mechanical overrule of the current blood flow. Now in her case we can nicely follow this. every time she stops and start. / mechanical compression , followed by a decompression and increase in tHb due to a great or good blood flow caused by the cardiac output and any additional vasodilatation effect.Now this in these graph for sure till about 420 . Than we have some questions for a close look , whether the small dip in tHb before stop is a occlusion outflow or a reaction due to jumping of the treadmill.We will get to that later. Y Think already how we would separate a jump reaction versus an occlusion outflow ? What we see as well is that at rest tHb goes steady up and up till to the last 2 steps where we have during the load a drop in thB as well no additional increase in tHb at rest. Indication. CO and vasodilatation in the load are now overruled form forces who do not allow anymore as good of a blood flow. In simple ideas 2 option. 1 mechanical so immediate to see when we go closer or systemic as a vasoconstriction due to different reactions. This are the tow simple basic ideas you look . 1 immediate so mechanical most often, versus delayed so system reason. So let's make a short stop here to digest this but not before we look one real good point

Unfortunately don’t have Moxy yet, to try the experiments above. Again, if the answers above are correct, then I am confused about the case of top endurance athlete (and for which Rachel's picture is similar according to her) where SmO2 values are persistently high implying that transfer of O2 from lungs to blood is good, but transfer from blood to muscle cells not as good (as this would imply CO2 too low, not CO2 too high).

The interesting and great section of this is where SmO2 values are persistently high implying that transfer of O2 from lungs to blood is good, but transfer from blood to muscle cells not as good

First part is absolutely understandable. We have a great cardiac output as well in the most section of the assessment a good respiratory action so great loading fro lungs to the blood . Indications would be as well a simple SpO2 sensor..If Ryinc and Rachel sent me on my email their home addresses I will sent you a free SpO2 sensor a thank you for your open debate here.

So far so good great delivery till perhaps some slight problems toward the last to loads.

but transfer from blood to muscle cells not as good

Well we do not know that based on what we see. What we k now is that she is running so it seems she uses nicely O2 form blood to cell but she simply delivers much more than she needs or at least till to the last 2 loads so we do not get a situation, where she needs to use a great utilization because there is less supply than what she needs. Let's try in different words. Delivery means we deliver blood to the needed area and hopefully this blood is saturated with O2. There are different reason why this may be not optimal and one of the more common once in sport is the not optimal loading of IO2 from the lungs to the blood due to the O2 disscurve. The first place to see this is the SpO2 sensors. Now we may or may not see a reaction in the mussel. If the O2 we nevertheless still delivery is more or balance d at what we need for the current activity , than SmO2 will not react. If we have an activity who needs a certain amount of O2 and due to either natural or manipulation of the O2 disscurve we can not load as much we will see d drop in SmO2. So utilization kick in which is now more than delivery. If utilization I less than delivery we have always a high SmO2 but that does not mean we do not utilize we just can not see it as easy. Now in some sports like perhaps ultra long distance running we hope to see the drop in SmO2 very very late in the assessment as we hoe we have as much a possible a great delivery to always keep utilization happy. A drop indicates that the " end " is coming a you use more O2 than you can delivery and that is not what you aim for in endurance sport > ( exceptions ) for all cyclists. In many for sure very high performance sport the tactic is taking over. Remember M Farahs' 5000 m run. Here we need as goo as delivery as possible so he has always more O2 than he needs and at the end we need an optimal utilization. meaning he can accept the feeling of a steady dropping SmO2 to very low levels. Same in cycling, where we may need to close a gap or stay in the group at the end of a hill otherwise the draft is gone. So in this cases you would like to see a long increase in high SmO2 but as well at t the end the ability to dig in and use as much O2 as possible Utilization. On the other side in ice hockey we know we will create a delivery problem so we need the ability to deoxygenate utilize as fast as accepted but as well need the ability to reload as fats as possible, So in Rachel's case we have a great delivery and by the end speed in here assessment we start to drop out of balance with delivery and go towards a g higher use than delivery. I sit good that she can not utilize very low. Yes and now. If she is on a level where mainly finishing the distance is the goal and improving her personal best , than we not really have to see a very low desaturation ability as this would give a few seconds or min at the end versus many minutes when we work on increasing the balanced SmO22 situation. When is it more important? If in her races there is a some tactical games to stay or split a group or in an end sprint.

So what we look is in an assessment, what creates really this shift form okay O2 delivery and utilization to a change of a higher rO2 use than delivery. Summary. This is really what we did all along over all this years. Looking for this magic Threshold , where O2 delivery and O2 utilization is just balanced and where it moves towards more O2 use ( Anaerobic ) and therefor there is a time limit how long we are able to do this. Now that section when we reach higher use than delivery is the section, where a better working utilization allows you to use more and therefore longer O22 so you may win the end sprint as you need O2 for sufficient ATP maintenance and energy supply . So next up will be exactly that can we find with the data we have the reason why Rachel got out of O2 supply an demand balance and what physiological system or reason created this. That would be at least on the day of her assessment the limiter and perhaps we can find out how she tried to compensate for the last few load s and with what system could she do that. This would be the compensator. So please jump in , where I lost you or may have not a good explanation.

Juerg, quick question. Since the O2 drop follows the decreasing tHb trend, how can I, and others, determine situations like at end of Rachel's 5/1/5 are ACTUALLY increasing O2 utilization and NOT more or less another sign of decreased supply ?

Fred , well not surprising for me that this great question comes from your side . Thanks. It is in fact a question to ask. If we look SmO2 as an indication of either : a) oversupply or less demand than supply , than we have normally an increase in SmO2. like we can assume a the start.b) if we have a balanced supply and demand we can see a flat SmO2 on all different levels so with a value of 85 +- but as well with a value of perhaps 30 +-. Similar to lactate user and MAXLASS where we can have a stable lactate by 2.4 or by 6.2 and so in. It is the situation, where we do not know how much we produce and how much we reuse there as well. So in SmO2 trends we may go very hard and have a delayed delivery so SmO2 drops down and than we may just get into a balanced supply and demand so we may stay on that relative low value.c) we use more or demand more than we can supply O2 drops.

So the question Fred has :increasing O2 utilization and NOT more or less another sign of decreased supply ? .

We may assume that when we go harder we may ask foo a higher utilization in a step test as we increase the demand to maintain ATP levels. So we can relative safely assume the utilization may increase. BUT not always because we may in fact have a local limitation and we may shift to other not assessed muscle groups to maintain or increase performance. So in this case we do not increase demand but may try to hang on what we have so same utilization and often same performance or muscle contraction so SmO2 will get flat. If we have a reduction in motor units and push the same we often see in this muscle a occlusion trend.

But we in fact can have an increase in utilization but as well a decrease in supply. Example SV drop, example increase n muscle contraction.so higher compression so less flow which leads than to decrease in SV as a feedback. Now if the contraction is really very high w e may actually start an occlusion trend so tHb will go up and we see the feedback when we release ( occlusion outflow ). if we increase but only compression so we will reduce back flow and therefor SV we see that as well when we stop as cardiac output is a systemic reaction so we have a decompression which will in the rest increase tHb but we have a delayed SV reaction whci9h means the tHb in the rest will not peak up to the levels before. In Rachel's case we have this in the last 2 rest look how tHb always over shuts the previous rest tHb level in the last 2 last one we miss due to stop of data collection w have a trend of a maximal tHb . The above can be one reason and or we reach a capillary maximal ability of blood flow or volume. Now decrease in supply could as well be due to a respiratory limitation as we may change to a much higher RF but ass we have a limitation in VE we may reduce therefore TV. So we have a much higher % of dead space air we move and we will create a hypercapnic situation. Now again this would be a systemic reaction so delay at the moment we stop. The reaction to expect . SmO22 drops despite the fact that we stop the O2 disscurve still for awhile on the right side so take O2 but hard to load in THb no muscle contraction and this is supported by high CO2 vasodilatation so fats and overshoot of tHb at the rest stage.

Now this sounds all great in theory but can MOXY / NIRS really back this up. That's where we used physio flow ( check CO reactions, SEMG check recruitment trend, Check lactate ( not sure why anymore ) but we thought we need lactate as a feedback .so lots of poking with minimal information. Cheeked VO2 reactions including CO2 and than compared the reactions of all the above with NIRS trends and NIRS trend in different depth when we use Portamon and MOXYNow many feed backs will show up in the extremity as we can afford O2 reduction easy in this area and far before we get into O2 sully problems in vital systems. Even nicer is to follow this idea in non-involved muscles. So you see what we have to do . We have to check the last few steps and see, what may change at the 1 min rest and reload level. Now it is your task to tell yourself or discuss on here what you see. So below the last levels and you see the time markers so the last 4 steps or lauds. first 3 and 4 last.So what do you see in reactions ?

Now the next picture is the next tow loads last loads at the 1 min rest and reload situation second last step reaction

And below last step reaction Now allow me one simple question to all Wattage user and Lactate threshold defender and VO2 max calculator. I used all of this ideas ,but please tell me where and how you found anything even remotely close to what we can see with NIRS. Than compare the price you pay for any of the equipment we all used and what did you really physiologically achieved in the direction of individual findings in your client.. For me it is fascinating after all this years to get involved in debates with all this classical ideas and even more fascinating is the level of aggression I often get when debating this issues now. Most interesting is than the next step. The step , where people see the potential value they can ad to their assessment ideas. ( BUT than they find a LIMITER like for ample respiration or right cardiac ventricular limitation. So they suddenly actually have the reason of stagnation or loss of performance but now . How to train that now as we know the limitation. In the pats no problem with that you open your cookbook you take your calculator and you load by xt % and the discussion is over. If you progress you are happy but if not ??? So the question is why do we have this discussion and why do we not embrasse this potential and work on it. What it needs is some time commitment to get into the thought process and as many regular readers proof to me it is possible . Look at great feedbacks form Daniele and many mails I am getting daily. True it is far from perfect but it may be a step in a new direction in individual quality coaching. Chef versus franchise all over again. Fred an all thanks for giving me a chance to think loud here.

I'm loving this feedback. I keep rereading and trying to extract as much as I can. And Sandy is doing a fabulous job helping to explain it to me as well. Thanks for sharing all this Juerg. It's very fascinating. I gave my moxy to Sandy today so she could grab the data for me so as soon as she can or as soon as she sends it to me I'll post the file from my Co2 run.

That sounds nice and if Sandy can sent the csv files than I can take some of the work of from her and we can look at here together. Hope to be back later today an show some close ideas on the last few pictures form you with the indication of what that all means. Sounds fun and crazy when we talk about a CO2 run does it. Different way how define training goals and specificity. We can run a with a fixed HR or a fixed performance but do we know what we may trigger , of we can make as you shows easy and nicely a specific idea and target and than go back and see, whether it triggers a change and if yes is it the change we have planned for or not. In any case, if we know what we stimulated and how we stimulated the idea , than we know that the result I form this no matter whether it is what we were hoping for or not but w e have an outcome feedback in physiological reactions. If it improves performance that is great if it is a step we have to do to built upon this and we have no performance improvement yet that is great as well as we may have expected it. One of the most intriguing reactions in that direction is the needed increase in vascularisation before we can se an increase in mitochondria density. So we ma have to accept a non increase in performance as we may need first a proper structural change to build upon this. Therefor n panic when we see we increase capillarisation and it is now a question o time before we see performance improvement.

Here is the graph of Rachel's CO2 run, Juerg I have sent the file to you through email. Rachel warmed up completely which is not hard as it has been 37 degrees and almost 100% humidity here. She then ran all out holding her breath for as long as she could. The goal was then to recover to the same blood flow (tHb) as reaching pre-interval SmO2 is never a problem. Rachel discontinued intervals (after 3) when breathing became hard to regulate. The dip in blood flow you see after the 3rd interval is her climbing a bridge.

During Rachel's assessment the following happened:-she jumped off the treadmill to grab a water bottle-I put the SpO2 monitor on her at interval 3 (it was 95), interval 4 (it was 89) and then at interval 5 where it read 95 again. (?? assuming this has to do with her compensator)-Rachel is a light heel striker however she has VERY little quad involvement when running which we have been working to change.

Did some experimenting with my moxy on my run today. I normally wear it on my quad but Juerg suggested (which Sandy already confirmed) that I don't run with my quads and perhaps a different placement might show other info. I started with it on my glutes (glute med) for the first half of my run and didn't see much difference than when I wear it on my quad. For the second half of my run Sandy suggested we try my hamstring, and volia I finally saw desaturation and it came with not too much effort. Sandy will post and send the csv files to Juerg sometime today.

Another intriguing thing happened through discussing the fact that I am clearly using my hamstrings. I have very, very tight calves ALL.THE.TIME and Sandy said that its probably the result of running with my hamstrings and it following through down the line. My hamstrings never bother me but she was showing me a hamstring specific stretch. When I tried the stretch I apparently created an occlusion and quickly desaturated from 89 to 77 and my blood flow decreased.

First Jeurg, thanks for following up on this case study. Rachel (and Sandy) thanks for sharing the data and permission to discuss it.

You asked a number of questions that i would like to try have a go at answering - remember no/limited experience in assessment so might be completely wrong!Think already how we would separate a jump reaction versus an occlusion outflow ?

I would expect that in an occlusion outflow, bloodflow would slowly increase (due to pooling), At the same time, Smo2 would most likely start decreasing as a trend because deoxygenated blood is not escaping. Then at the point where load is removed - blood flow would suddenly increase due to occlusion being released and because deoxygenated blood is now released, Sm02 would increase reasonably quickly.

On a jump reaction. I would expect that there might be a more sudden blood flow impact. Due to immediate muscle compression, blood flow would probably fall and then as muscle decompresses it would rise again. Similarly Sm02 would probably drop at the point of jump, but then rise quickly again as utilisation falls away.

Now Rachel's case In relation to the last few loads that you put up Comparing the 3rd/4th last loads vs the last loads, the key differences to me seem to be: 1. tHb decreasing in the last loads, but not in the loads before. 2. In the last loads, on rest tHb increases immediately, but there is a lag to Sm02 recovery - it actually continues to fall slightly after the load is removed.

Now on number 1 above (thb decreasing in last loads) As you explained, there seem to be two possibilities - either an immediate mechanical reaction or a slower systemic type of reaction. To me in this instance it does not look immediate, it looks like a trend - so it seems to be a systemic reaction?

On number 2 (lag Smo2 recovery) - First we know load has been removed. - It is possible that Smo2 keeps falling because muscle has not relaxed and therefore utilisation does not fall away completely. However, to me this seems unlikely given that we know thb does increase immediately. - So what other options, for Sm02 slow recovery-Reduced cardiac output - does not seem likely given that tHb increases immediately when load removed.- So that leads to the respiratory problem possibility that Rachel/Sandy Jeurg highlighted? Would the correct interpretation be here that Rachel's diss curve has shifted to the right because CO2 too high so more difficult to transfer 02 into blood, and takes some time after load removed to recover? (also noting that the last graph Sandy posted also seems to show a fall in Sm02 and slow recovery when holding breath = CO2 increase).

I was watching the new "intro to muscle oxygen monitoring" videos last night and there was one part where Jeurg discusses muscle contraction and creating an occlusion but in the context of strength training.

My question is are you creating that same contraction when doing a stretch (it wasn't an extreme hamstring stretch, I felt it but it wasn't painful) and why would this happen?

I have been having what probably is compression syndrome issues with my calves where my feet get tingly/go numb after running for awhile. My calves are super tight and I am having lots of trouble getting them to release. Can I use the Moxy to help and figure out what is happening in this situation?

Great info Rachel. 1. I will explain in short here the tHb reaction in connection with compression.

1a) compression due to outside influence. Occlusion workouts is the most extreme option where we can create a arterial occlusion IN this case tHb doe snot react as w have no inflow and no outflow but just what is in the occluded area.. Ope who choose this strength training idea would benefit from using MOXY as in many cases we sse muscle actual be damaged due to a too long occlusion time.

Now different situation for occlusion trends. . or better blood flow restriction. I will later show this step by step in your assessment so it may be even easier to understand it there. As well as we will use in your case tHb as a guide as well for your live workouts. Now here in very simple wording. You have a blood vessel or blood vessels. You have to type of vessels Arterial or venous flow. In stupid simple terms the arterial vessels have a higher quality and are very elastic and therefor you need more pressure before you inlfcunce the lumen in this pipes. The venous vessels are less quality in the way of elasticity and therefore less pressure needed to start restriction flow there. ( That's why you have an upper and lower Blood pressure to read out. so you start muscle contraction you create pressure form outside and tHB will drop. The reaction often is a CO increase and if the pressure from you heart is higher than the compression tHB will go back up again. You push harder so CO can not overrule the compression and tHB will keep dropping. If the pressure exceeds a certain mmHG you start to reduce the outflow (veneous occlusion trend and more blood comes in than can go out and tHB goes up occlusion pooling. The most pooling is when venoeus system is completely compressed. If you keep increasing pressure you start to reach an arterial c occlusion and tHB stops going up. If you release a bit you have again inflow and no outflow so tHb goes up. If you increase alot than you have again an outflow and THb will actually drop as an occlusion outflow reaction.

Now think what happens if you do a certain type of stretching and what is the result of it? Will be back on these interesting conflicting habits later. Stretching to the limit or the limit of stretching in sport. A long lasting an ongoing disucssion based often on myth than actual facts.

Here is Rachel's Saturday run.Closer look at the second half of run where we placed it on the hamstring.Followed on Sunday with a short hamstring run (easy pace) and a leisurely group bike ride broken n two parts.

Sandy great work as usual. Again can you sent the csv files and we can go even deeper into the discussion. As we can see short hand vastus lateralis is a minimal involved muscle but we can still use this for the limiter compensator ideas but the other info here much nicer for " zoning" or what ever we like to call it. Greta great work and I will dig in to get Rachel ideas together with you into a deeper discussion. Cheers Juerg

I know this is not a physiology class, but I am trying to understand something.

You say:"In stupid simple terms the arterial vessels have a higher quality and are very elastic and therefor you need more pressure before you inlfcunce the lumen in this pipes. The venous vessels are less quality in the way of elasticity and therefore less pressure needed to start restriction flow there. (That's why you have an upper and lower Blood pressure to read out. so you start muscle contraction you create pressure form outside and tHB will drop. The reaction often is a CO increase and if the pressure from you heart is higher than the compression tHB will go back up again."

What I understand from a bit of reading and from your description:Arteries are more compliant (more flexible).Arteries will allow for higher rate of blood flow because they are better able to expand to accomodate increased internal pressure, so under normal conditions they can accommodate higher flow rate.

Veins are less compliant (less flexible).Veins will not allow for as much blood flow because they do not expand as well (the restriction flow you talk about).

Example:Soft latex tube = Artery.PVC tube = Vein.

Occlusion occurs when for instance:External muscle contraction applies pressure to the artery or vein.

What I would expect to see:Arteries normally allow for higher THb rate of flow because they can expand to allow for higher volume, but are more susceptible to occlusion because they compress more easily.Veins normally allow for less Thb to flow because they do not expand well, but will be less susceptible to occlusion because they do not compress as quickly.

What I don't understand:Arteries deform easier to allow blood flow, so why should they not also compress more easily when external (muscular) pressure is applied?Why are veins not more resistant to EXTERNAL compression/occlusion if they are more "rigid"?

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